Inflammatory bowel disease (IBD) – which includes Crohn’s disease and ulcerative colitis—affects about 3.1 million adults in the US.
The disease can cause debilitating symptoms such as diarrhea, stomach ache and cramps, blood in the stool and more.
Now, researchers at the UK’s Francis Crick Institute, working with UCL and Imperial College London, have discovered a genetic component – referred to as a ‘weak spot’ in DNA – that is present in 95% of living with this disorder.
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The study, published in the journal Nature earlier this month, identified a piece of DNA that increases the activity of a gene called ETS2.
ETS2 has been linked to inflammatory functions that increase the chances of IBD.
Rosario Ligresti, MD, chief of the Division of Gastroenterology at Hackensack University Medical Center in New Jersey, was not involved in the research but called the findings “pretty important.”
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“Researchers have finally shown that all autoimmune and inflammatory diseases — including IBD — appear to be caused by a single gene, ETS2,” he told Fox News Digital.
“Research identified this gene as a central regulator of a type of inflammatory cell called a macrophage, which is the key inflammatory cell in all of these processes.”
“IBD usually develops in young adults and can cause severe symptoms that disrupt education, relationships, family life and employment.”
“The more the gene is ‘turned on’ or amplified, the greater the risk of inflammation. Without this gene, these cells do not ‘turn on’ and there is no IBD.”
until diet and stress Long suspected of making IBD worse, “the exact ‘molecular switch’ that activates inflammatory bowel disease has been unknown until now,” Ligresti noted.
“This discovery is so exciting and significant because it only gives us a better understanding of the inner workings of the disease and will allow researchers to adapt existing drugs to eventually treat it,” added Ligresti.
The research team is now investigating drugs that can reduce the activity of the ETS2 gene, thereby reducing the occurrence of IBD.
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They found that an existing group anti-inflammatory medications inhibitors called MEK can do the trick.
“Although there have been many suggested risk factors for IBD, there is currently no way to prevent the onset of IBD,” Ligresti said.
“We do know, however, that inflammatory pathways in the body are likely to be activated at least five years before the onset of IBD symptoms.”
Ideally, he said, patients at increased risk could be given a drug during this time period that could “catch IBD early.”
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While more research is needed to find ways to deliver these MEK inhibitors to target cells, Ligresti noted that this discovery opens a “tempting door” to the future of highly effective therapies to “smother” inflammatory bowel disease.
James Lee, group leader of the Genetic Mechanisms of Disease Laboratory at the Crick, who led the research, agreed that better treatments are “urgently needed”.
“IBD usually develops in young adults and can cause severe symptoms that disrupt education, relationships, family life and employment,” Lee said in a Crick press release.
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“Using genetics as a starting point, we have discovered a pathway that appears to play a major role in IBD and other inflammatory diseases,” he said.
“Excitingly, we have shown that this can be targeted therapeutically and we are now working on how to ensure that this approach is safe and effective for the treatment of people in the future”.
Lauren Golightly, 27, was diagnosed with Crohn’s disease in 2018 after experiencing stomach cramps, bleeding and irregular bowel habits, according to the release.
“I’ve had a difficult road since the diagnosis, with a lot hospital admissionsseveral different medications and even surgery to have a temporary stoma bag,” she said in the release.
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“I still have breakouts and can still spend a lot of time in the hospital.”
She also said, “Learning about this research is so exciting and encouraging. I hope it can make a difference for me and the hundreds of thousands of other people living with IBD.”
Fox News Digital reached out to the researchers for additional comment.
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